Exam 2: Thrombocytes, Hemostasis, and Alterations in function Flashcards
1
Q
Thrombocytes
A
Platelets
2
Q
Thrombopoiesis
A
Stimulated by thrombopoitein
3
Q
Thrombopoietin is a
A
Hormone growth factor produced by liver, kidney, bone marrow
4
Q
Do thrombocytes have a nuclei?
A
No! they do not have a nucleus
5
Q
While thrombocytes lack a nuclei, they have
A
organelles and enzyme systems for generating energy and synthesizing secretory products, which are stored in granules dispersed throughout the cytosol
6
Q
Thrombocytes contain high concentrations of
A
actin and myosin
7
Q
Thrombocytes are disc shaped and are
A
metabolically active cytoplasmic fragments of megakaryocytic
8
Q
Thrombocytes (platelets) contain
A
granules in which many of the chemical mediators of hemostasis reside
9
Q
Primary function of thrombocytes
A
Hemostasis
10
Q
Thrombocyte count
A
150,000 - 400,000 / mm^3
11
Q
Where are additional thrombocytes stored?
A
Spleen!
12
Q
Life span of thrombocytes
A
7-10 days
13
Q
Thrombocytopenia
A
Platelet count of < 150,000 /mm^3
14
Q
Thrombocytopenia is caused by
A
Decreased platelet production
Decreased Platelet survival
Increase Platelet consumption in spleen
Dilution
15
Q
Normally, spleen reserve about 30% of platelets, an enlarged spleen will reserve
A
up to 90%
16
Q
How does dilution contribute to thrombocytopenia
A
Overload of fluids, for example, from massive transfusions of whole blood that has been stored > 24 hours (platelets degenerate in stored blood after 24 hours)
17
Q
Clinical manifestation of Thrombocytopenia
A
- Increased bruising and prolonged bleeding following minor trauma
- Petechiae, purpura, and ecchymosis
- Spontaneous mucosal (gingival bleeding, epistaxis [nose bleeds] ) gastrointestinal and/or intracranial bleeding
18
Q
Petechiae, Purpura and ecchymosis are
A
Leakage of blood cells into skin or mucous membranes
19
Q
Petechiae are
A
tiny, pinpoint blotches
20
Q
Purpura are
A
blotches that are larger
21
Q
Ecchymosis is redness that is non-blanchable (outside of vessels) and when
A
Petechiae and Purpura are combined
22
Q
Any bleeding into the skin that is > 1 cm is called
A
Ecchymosis
23
Q
What clinical manifestation can be seen when platelet count is 50,000 / mm^3
A
Increased bruising and prolonged bleeding following trauma
24
Q
What clinical manifestation can be seen when platelet count is <50,000 / mm ^3
A
Petechiae, purpura, and ecchymosis
25
What clinical manifestation can be seen when platelet count is <20,000 / mm ^3
Spontaneous mucosal gastrointestinal and/or intracranial bleeding
26
Type of thrombocytopenia that is chronic and autoimmune
Immune thrombocytopenia purpura
27
Immune thrombocytopenia purpura is a
Chronic, autoimmune disorder, and is the most common cause of thrombocytopenia secondary to platelet destruction
28
What does Immune thrombocytopenia purpura do to platelets?
Formation of antibodies against platelets cause destruction of platelets in spleen
29
Patient presentation of Immune thrombocytopenia purpura
History of epistaxis, bruising, petechiae, purpura, bleeding gums, Melena (blood in stool), splenomegaly (enlarged spleen)
30
Treatment of immune thrombocytopenia purpura
Bleeding precautions (avoid giving injections, electric razors, etc.)
Immunosuppressants
corticosteroids (usually prednisone)
Splenectomy
Patents with platelets > 30,000/mm^3 often do not have increased mortality related to thrombocytopenia
31
Thrombocythemia aka
Thrombocytosis
32
Thrombocythemia, generally defines as
Platelet count > 400,000 mm^3 but usually not clinically significant until >750,000
33
2 types of thrombocythemia
Essential (primary) thrombocythemia
| Secondary thrombocythemia
34
Most common thrombocythemia
Essential (primary) thrombocythemia
35
Essential (primary) thrombocythemia
Myeloproliferative neoplasm (cancer of bone barrow cells)
36
essential (primary) thrombocythemia increase
Platelet production and often accompanied by increase of RBC production
37
secondary thrombocythemia may occur after
Splenectomy, may be gradual, up to 3 weeks post op
38
Why does secondary thrombocythemia happen after a splenectomy?
Short term platelet increase in system as body toys to recalibrate
39
Reactive thrombocythemia *secondary
due to inflammatory conditions
| cause is underlying condition like infection
40
Clinical manifestations of thrombocythemia
```
Increase WBC
Leukocytosis
Splenomegaly
Thrombosis
blessing
itching
microcirculatory symptoms, leading to ischemia in the fingers, toes, to CV regions
Erythromyalgia
headache
paresthesias
```
41
Pathophysiological elevations in thrombocythemia may result in
```
Thrombosis (DVT, Peripheral vascular ischemia)
Thromboembolic events (pulmonary embolism)
```
42
Mechanisms of hemostasis
Stopping blood flow
43
Endothelium
a type of epithelial cell that forms a single later along the inner lining of blood vessels
44
The endothelium represents a
dynamic interface between flowing blood and the vessel wall, and produces a variety of factors that REGULATE BLOOD FLUIDITY
45
he endothelium regulates the fluid state of blood through
its thromboresistance and profibrinolytic properties, and anti-inflammatory potential
46
Nitric oxide
naturally occurring gas released from vascular endothelial cells that causes vasodilation
47
Prostacyclin
- type of prostaglandin involved in the normal vasodilation at rest
- anti platelet activity
48
Endothelin
peptides that leas to vasoconstriction
49
How does endothelium respond to injury
pro clotting attributes (vWF assists in platelet adhesion)
50
Steps of hemostasis
1. Vascular spasm
2. platelet plug formation
3. coagulation (extrinsic and intrinsic)
4. clot retraction
5. fibrinolysis
51
Vascular spasm is a response when
there is a break in the vessel wall
52
Hemostasis is
immediate and temporary response
53
hemostasis is a ____ reflex
Neural reflex
54
in vascular spasms, what humoral factors contribute to spasm
Humoral factors such as endothelia, 5-HT, and TXA2 released from platelets contribute to spasm
55
Overall, vascular spasms causes
Decrease in blood flow through vasoconstriction
56
Damaged vessel contains collagen, which attracts
platelets
57
Von Willebrand factor (vWF) is released from the endothelium which
binds to platelet receptors, causing platelet adhesion
58
When platelets are activated, they become
- Enlarged and become irregularly shaped
| - Form numerous spiky projections, become sticky, and expose glycoprotein receptors
59
Activated platelets expose
glycoprotein receptors
60
Activated platelets degranulate and release
ADP, 5HT, TXA2, which furthers VASOCONSTRICTION
61
Accumulation of large numbers of platelets cause
platelet aggregation which forms a mass called the platelet plug
62
are platelet plugs temporary or long term?
they are a temporary repair and is referred to as primary hemostasis
63
Primary hemostasis is
a temporary repair
64
clotting pathways of blood coagulation
Intrinsic pathway
| extrinsic pathway
65
Intrinsic pathway:
all elements for clotting are present in the blood
66
Extrinsic pathway
requires factor III (tissue thromboplastin) which comes from tissue
67
Intrinsic and extrinsic pathway combine to become
common pathway
68
Blood coagulation involves conversion of
fibrinogen to fibrin
69
Fibrinogen is a
protein always present in plasma
70
Fibrin
Forms a meshwork that traps RBC & platelets ---> clot!
71
The production of fibrin is referred to as
secondary hemostasis
72
Both clotting pathways happen
simultaneously
73
What makes clotting permenany
When fibrinogen is converted to fibrin
74
The common pathway begins with
Prothrombin converts to thrombin, to then convert fibrinogen to fibrin
(Basically as factor 10)
75
What factors works on prothrombin
activated factor 10
76
Most clotting factors are synthesized in
the liver
77
what clotting factors are synthesized in the liver
II, V, VII, IX, X, XI, XII
78
What factors are vitamin K dependent
Factors II (prothrombin)
VII
IX
X
79
The chief sources of vitamin K are
Synthesis by bacteria in large intestine
| Dietary (green foods)
80
Now that the clot is more permeate, what makes it stronger
clot retraction step
81
Clot retraction involves
Consolidation and tightening of fibrin clot
82
What pulls the edges of damaged tissue together
Contraction of actin and myosin in platelets pull edges of damaged tissue together
83
Platelets in clots...
bind fibrin threads together
84
What is squeezed out in the process of clot retraction
serum (plasma without fibrinogen & clotting factors)
85
In the clot retraction process, platelets release
Factor XIII
86
Factor XIII does what
strengthens and stabilizes the clot
87
Clot is usually dissolved within a few days after clot formation by
fibrinolysis
88
What happens in fibrinolysis
Slow release of tissue plasminogen activator (t-PA) from injured tissue converts plasminogen to plasmin
89
Plasmin (enzyme) causes
Dissolution of the clot
90
Plasmin chops through fibrin and
digests fibrin threads and inactivates clotting factors
91
Disorders of coagulation
```
Vitamin K deficiency
Liver disease
Venous thromboembolism
Pulmonary embolism
Von Willebrand disease
Hemophilia
```
92
Vitamin K is a
Fat-soluble vitamin
93
where is vitamin K stored
in the liver and fat tissue
94
Vitamin KK is necessary for the
synthesis and regulation of prothrombin
95
Most common sources of Vitamin K is
green leafy vegetables
96
Primary reason for vitamin K deficiency is
Total parenteral nutrition (TPN) with antibiotics that destroy the GI flora
97
Liver disease may include
Hepatocellular disease, cirrhosis, etc.
98
What site is where most of clotting factors are produced
Liver
99
Damage to the liver cells leads to
significant decrease in most clotting factors (Factor VII)
| diminished levels are clotting system regulators (antithrmbin)
100
Challenging clinical manifestions in liver disease
Thrombocytopenia
| Pooling of platelets in the spleen, often leading to portal hypertension
101
Thrombosis is
hemostasis in the wrong place
102
A thrombus is a
stationary blood clot in the cardiovascular system (VENOUS OR ARTERIAL)
103
Predisposing factors for thrombus formation
Stasis
Hypercoagulability
Endothelial damage (vessel wall/abnormality)
104
Two manifestations of venous thromboembolism (VTE)
Deep VEIN thrombosis
| Acute pulmonary
105
2 categories of deep vein thrombosis
Distal (calf) vein thrombosis, in which thrombi remain confined to the deep calf veins
Proximal veins thrombosis, in which thrombosis involves the popliteal, femoral, or iliac veins
106
Which is clinically of great importance, distal or proximal vein thrombosis
Proximal vein is of greater importance clinically, since it is more commonly associated with the development of PE
107
What can happen from a proximal vein thrombosis
Can follow venous flow into right side of the heart and get longed in the pulmonary vasculature and cause acute pulmonary embolism
108
Risk factors for venous thromboembolism
```
Recent surgery
History of immobilization (long haul travel) or prolonged hospitalization/bed rest
obesity
Prior episode of venous thromboembolism
lover extremity trauma
malignancy
oral contraceptives
pregnancy or postpartum
peripheral vascular disease
diabetics
lung disease or who smoke
```
109
Pulmonary embolism
Life threatening complication of venous thromboembolism
110
Thrombus becomes an embolus when it is
no longer stationary
111
Embolus tend to travel
towards heard
| Cardiac circulation --> pulmonary artery --> lungs
112
Large percentage of pulmonary embolisms (PE) are
clinically silent
113
Pulmonary infarction occurs in up to
20%
114
Pulmonary embolism is fatal in
1% patents
115
DVT is associated with >600,000 US hospitals annually and result in
> 200,000 death from pulmonary embolism
116
Von willebrand disease
An inherited blood-clotting disorder
117
Von villebrand disease is an
autosomal dominant, three type, 20 variants
118
one of three types of von-willebrand disease is
Autosomal recessive, vWD type 3
119
The most common type of vWD
type I
120
vWD is characterized by
Von willebrand factor
121
Von willebrand factor is a
plasma protein
122
What does von willebrand factor so
helps platelets stick to injured blood vessels during formation of blood clots (builds a bridge activated platelet & endothelium from platelets)
123
vWF also is a carrier and stabilizer for
Factor VIII
124
deficiency of vWf also means
deficiency inhibits multilevel clotting factors
125
Patient presentation of von willebrand disease
Evidence of mild ecchymosis (discoloration under skin)
| Bleeding (nose, gums, GI, menorrhagia) with NORMAL platelet count
126
treatment of von willebrand disease
Bleeding precautions
avoidance of aspirin
DDAVP (vasopressin) which stimulates release of stored vWF from endothelial cells
----LEADING TO VASOCONSTRICTION + FLUID RETENTION
127
Most classic hemophilia
Hemophilia A "classic hemophilia"
128
Hemophilia is a
X-linked disorder (or may arise from a new mutation of the F8 gene)
129
Hemophilia A is caused by
mutation on the F8 gene that provides instructions to make factor VIII
130
Hemophilia causes a
lack of VIII factor
131
A lack of factor VIII causes
```
spontaneous bleeding into soft tissues, GI tract, Hip, Knee, elbow, ankles
inflammation
pain
swelling
bruising
deformities
immobilization
bleeding into brain from brain injury
```
132
hemophilia mutant gene is on
X chromosome
133
Most affected persons of hemophilia are
male, affected females are extremely rare
134
As a X-linked inheritance
all affected males never transmit gene to sons
| all daughters of an male are carriers, none are affected
135
Sons of carrier females have
50 % chance of inheriting it and being infected
136
Daughters of carrier females have
50% of inheriting and carrying
137
managements of hemophilia
infusions of factor VIII (human or recombinant)
138
for mild disease of hemophilia: management
Desmopressin acetate (DDAVP)
139
Desmopressin acetate (DDAVP) stimulates
release of vWF from endothelium which increases factor VIII levels 2-3 fold
VASOCONSTRICTION)
140
hemophilia pateitns should
Avoid contact sports
| bleeding precautions
141
aPTT
Activated partial thromboplastin time
142
aPTT evaluates the
intrinsic and final common pathways
143
aPTT is the
length of time for blood to clot
144
Normal value for aPTT
30-40 seconds
145
What medication increases aPTT
Heperain
146
Those on heparin, aPTT labs should be
1.5 0 2.5 times the normal range is considered therapeutic level
147
With heparin, we are looking for
prolonged aPTT because we want decrease risk of clotting
148
PT
Prothrombin time
149
PT evaluates the
extrinsic and final common pathway
150
PT is
the length of time for the blood to clot
151
Normal time for PT
10-14 seconds
152
Those on warfarin, PT labs would be
1.5-2.5 times the normal range to be considered therapeutic
153
INR
International normalized ratio
154
When patent that takes medication that acts on extrinsic factor, check
PT and INR
155
INR evaluates
extrinsic pathway, but provides uniformity worldwide (independent of reagents)
156
INR is most often used to monitor patent on
warfarin
157
1.5 INR
low level anticoagulation (Prophylaxis)
158
2.0-3.0 INR
Medium level anticoagulation (DV, stroke, PE, prophylaxis, MI)
159
2.5 - 3.5 INR
High level anticoagulation (DVT, mechanical heart valve)
160
High alert medications =
Medications that have the highest risk of causing injury when miused
161
Top 5 high alert medications
```
Insulin
Opiates
Injectable potassium chloride
Anticoagulants
Sodium chloride solutions above .9%
```
162
Safety goal for anticoagulant medications
reduce the likelihood of patient harm associated with the use of anticoagulation therapy
163
anticoagulation therapy is used for a number of conditions, including
Atrial fibrillation
Deep vein thrombosis
Pulmonary embolism
Heart valve replacement
164
Anticoagulant medications are more likely than other medications to cause harm due to
complex dosing, insufficient monitoring, & inconsistent patient adherence
165
Healthcare organizations that provide anticoagulant therapy MUST have
a process in place to reduce the risk of anti-coagulant associated patient harm
166
types of coagulation modifiers
Anticoagulants
Antiplatelet agents
Thrombolytics
167
Overall, anticoagulants
prevent coagulation and clot formation
168
Overall, anti platelet agents
act on platelets
169
overall, thrombolytics
lyse clots
170
Anticoagulants are drugs that
prevent the formation of a clot by inhibiting certain clotting factors
171
Three main types of anticoagulants
Heparins
Vitamin K antagonists
Direct Thrombin inhibitors
172
Indications for anticoagulants
High risk of clot formation (MI, Unstable angina, AF, uses of indwelling devices (heart valves)
Major orthopedic surgeries
prolonged immobilization
173
Anticoagulants are also used in the treatment of
Ischemic complications of unstable angina, some dysrthymias, and disseminated intravascular coagulation
174
Heparin targets which pathway
Intrinsic pathway
175
Heparin mOA
Combine with antithrombin III (natural anticoagulant) to inactive clotting factors 9,10,11,12
which inhibit the conversion of prothrombin to thrombin
176
after thrombosis, heparin can also
inactivate thrombin, preventing the conversion of fibrinogen to fibrin
177
Adverse effects of heparin
Hemorrhage
Neurologic damage
Thrombocytopenia (heparin-induced thrombocytopenia)
Hypersensitivity reactions
178
Heparin half life
super short
179
Nursing considerations and adverse effects of heparin
Local irritation and hematoma from SQ injections
Hemmorage
Monitor for heparin induced thrombocytopenia
Monitor for hypersensitivity reactions (animal antigens): manifested by chills, fever, urticaria, anaphylaxis
180
antidote for heparin
Protamine sulfate
181
Protamine sulfate MoA
Binds with heparin to form a stable complex that can be eliminated
182
Signs of bleeding
```
Bruises
Petechiae
Red or black stools
Discolored urine
Pelvic pain
Lumbar pain
Headache
```
183
Black box warning for heparin
some heparin products contain benzyl alcohol (preservative)
Contraindicated in neonates (Fatal toxicity!)
USE PRESERVATIVE FREE HEPARIN
184
Enoxaparin drug class
Low molecular weight heparin (LMWH), anticoagulant
185
Enoxaparin is basically heparin that is
composed of shorter molecules that unfractionated heparin
186
Enoxaparin indications
Same as heparin
Prophylaxis/treatment of thromboembolism (especially with orthopedic surgery/bariatric surgery)
Adjunct to percutaneous coronary intervention
Unstable angina
acute coronary syndrome
187
MoA enoxaparin
Potentiates the effect of antithrombin III, making it a rapid INACTIVATOR of coagulation factor Xa, which inhibits factor Xa, inhibiting thrombin, thus the anticoagulant effect
188
Enoxaparin effects which pathway
Intrinsic pathway
189
Antidote for enoxaparin
protamine sulfate
190
Half life of enoxaparin
extended, so the dose is less often
191
Adverse effects of enoxaparin
similar side effects of heparin, bleeding less frequent
192
Protamine sulfate nursing considerations
Rapid administration can cause severe HYPOtension & anaphylactoid reactions (max 50 mg over 10 min)
Monitor vital signs closey during administration, monitor aPTT
193
Black box warning protamine sulfate
- Severe hypersensitivity reactions (hypotension, cardiovascular collapse, pulmonary hypertension, pulmonary edema)
- Risk increased with high doses, repeated doses, previous protamine administration
194
Warfarin drug class
Vitamin K Antagonist, anticoagulant
195
Warfarin effects which pathway
Extrinsic + Common pathway
196
Warfarin MoA
Acts int he liver to prevent synthesis of vitamin K dependent clotting factors (2,7,9,10)
197
Adverse effects of warfarin
```
Hemorrhage
Nausea/vomitting
Abdominal pain
Alopecia
Uticaria
Dizziness
Joint or muscle pain
```
198
Warfarin Nursing considerations
Monitor PT, INR (2-3 range), baseline, then at intervals
199
2nd most common drug
warfarin
200
Warfarin patient teaching
- Avoid situations that may result in injury, bleeding precautions (electric razors)
- Monitor for bleeding (gingival bleeding, tarry stool, bloody sputum, hematuria, internal bleeding
- INR monitoring
- wear medic identifications
- Dietary considerations
201
When taking warfarin, patients should do what with their diet
Keep diet CONSISTENT with foods that are high in vitamin K (avocado, broccoli, lettuce, egg yolk)
--- Increasing vitamin can decrease effectiveness of warfarin
202
OTC and warfarin patent teaching
Avoid taking over-the-counter NSAIDS, especially aspiring or drugs containing salicylates
--- basically avoid drugs that target COX 1
203
Antidote for warfarin
VITAMIN K
204
Heparin onset
RAPID (minutes)
205
Warfarin onset
SLOW (hours)
206
Dabigatran drug class
Direct Thrombin Inhibitors, anticoagulants
207
Dabigatran moA
direct and reversible inhibition of thrombin
208
Direct Thrombin Inhibitors have no known
antagonists
209
Dabigatran effects which pathway
Common pathway
210
Dabigatran indications
anticoagulation to prevent strokes
systemic embolization in individuals with nonvalvular atrial fibrillation
-- treatment and prevention of deep vein thrombosis and pulmonary embolism
211
Dabigatran adverse effects
```
Bleeding
Nausea
Vomitting
anemia
Hematoma
Elevated liver function tests
```
212
4 types of anti platelet drugs
Salicylates
Adenosine diphosphate receptor (ADP) inhibitors
Glycoprotein inhibitors
Arterial vasodilators
213
Aspirin drug class
Antiplatelet drugs, salicylates
214
Aspirin indications
inhibit platelet aggregation
| Reduce risk for: MI, Ischemic cerebrovascular accident, angina
215
aspring prevents reocclusion of
Coronary stents
216
Clopidogrel drug class
Adenosine diphosphate (ADP) receptor antagonist
217
Clopidogrel indications
- Prevent stenosis of coronary stents
- Decrease risk of death due to thrombotic events (MI, stroke, embolism) in patients w/ atherosclerosis
- Peripheral arterial disease history of MI and stroke
----- Decreases ADP aggregation which decreases platelet aggregation
218
Clopidogrel moA
IRREVERSIBLE blockade of ADP receptors on platelet surface, which prevents ADP-stimulated aggregation
219
Clopidogrel requires
biotransformation into active metabolite
220
Clopidogrel administration
PO only
221
Clopidogrel adverse effects
```
bleeding
dyspepsia
diarrhea
rash
chest pain
purpura
atrial arrhythmias
edema
GI hemorrhage
```
222
Clopidogrel nursing consideration
Monitor signs and symptoms of bleeding
Monitor Hemoglobin & hematocrit, platelets at baseline and periodically
Contraindicated in active blessing
Concurring use with NSAIDS, aspirin, and other anticoagulants may increase bleeding
223
When should clopidogrel be discontinued
discontinue 5-10 days before invasive procedures (as with any antiplatelet/anticoagulant)
224
What group of patients are poor metabolizers of clopidogrel
Patients with one or more copies of the variant CYP2C19*2 &/or CYP2C19*3
225
Patients with one or more copies of the variant CYP2C19*2 &/or CYP2C19*3 may have
lower reduced conversion of clopidogrel to its active metabolite
Lower active metabolite exposure may result in reduce platelet inhibition
226
abciximab drug class
Glycoprotein inhibitor, anti platelet
227
Abciximab indications
Patients undergoing coronary artery procedures such as angioplasty
228
Abciximab moA
Prevents platelets from sticking together (adhesion) and causing thrombus (blood clot) formation within the coronary artery
-- targets platelet adhesion, decrease sticky ability
229
Thrombolytics are used when
clot has been formed, and needs to be dissolved
230
Thrombolytics are coagulation modifiers that
lyse thrombi in the blood vessels to establish blood flow
231
Atleplase drug class
Thrombolytics
232
Alteplase administration
IV
233
Alteplase moA
a naturally occurring tissue plasminogen activator (t-PA) produced through recombinant DNA techniques
234
Alteplase indications
```
Acute MI
Arterial thrombosis
DVT
Occlusion of shunts or catheters
Pulmonary embolism
Acute thrombotic stroke
```
235
Alteplase adverse effects
Internal, intracranial, and superficial bleeding
| precipitate cardiac dysrhythmias
